Multiple sclerosis is an autoimmune disorder that targets the brain and spine. But certain drugs that have worked wonders for people with other autoimmune disorders – such as rheumatoid arthritis – make the symptoms for MS worse. Researchers think that they have identified why and the answer is in the genes.

The team from Oxford University identified a genetic variant that encodes the protein called tumor necrosis factor receptor 1, or TNFR1. Put simply, people of European ancestry who have two A’s in that section of the genome are 12 percent more likely to develop MS than people who have a pair of G’s there.

The protein identifies an immune molecule known as TNF that destroys cancer cells, but has also been implicated in immune diseases. In healthy bodies, the protein sits on the outside of cells and gives instructions to TNF molecules. But in certain people with MS, the protein is shorter and cannot access the TNF molecules. Drugs that block the protein exacerbate the symptoms of MS.

Researchers identified this information through a genome-wide analysis, which compared thousands of people with MS against people without the condition. By identifying genes that may increase the risk of a disease or increases drug resistance, researchers hope that better, more targeted, treatment for MS patients can lead to better treatment of the disease.

Multiple sclerosis is caused by damage to the myelin sheath, the protective coating of nerve cells. The damage is caused by inflammation when the body's immune system cells attack the nervous system. Despite the fact that the illness has been studied for more than 150 years, it is currently not understood why this happens. Researchers believe that genetics, a virus, or environmental factors may play a role. 200 million suffer from the illness all over the world.

The results of the study have been published in the most recent issue of Nature.

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